Aspirin reprograms platelet signaling and the intrahepatic microbiome to suppress RyR2-driven inflammation and fibrosis in preclinical chronic liver disease
overload, ER/mitochondrial stress (p < 0.05). Further, RyR2 blockade in HSCs reduced its activation by activated platelet secretome or TGFβ1 (p < 0.05). CONCLUSIONS: Platelet deactivation using aspirin regresses hepatic fibrosis by decreasing intrahepatic platelet accumulation/activation, inflammation and modulation of intrahepatic microbiome. Induction of RyR2 is critical for fibrosis development and pharmacological inhibition of RyR2 could ameliorate liver fibrosis.
Authors
- Jaswinder Singh Maras (ORCID: https://orcid.org/0000-0003-3938-362X)
- Adil Bhat (ORCID: https://orcid.org/0000-0003-3878-2514)
- Shvetank Sharma (ORCID: https://orcid.org/0000-0001-7139-2011)
- Anupama Kumari (ORCID: https://orcid.org/0000-0003-0579-5706)
- Shiv Kumar Sarin
- Sudrishti Chaudhary
Institutions
- Institute of Liver and Biliary Sciences (IN)
Publication Details
- Journal
- Biomedicine & Pharmacotherapy
- Published
- 2026-03-31
- DOI
- https://doi.org/10.1016/j.biopha.2026.119296
- Primary Topic
- Liver Disease Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Department of Science and Technology, Ministry of Science and Technology, India
- Indian Council of Medical Research
- Defence Science and Technology Group